Strokes are the world's leading cause of disability. About one-third of stroke survivors are permanently disabled one year after the acute event. About two-thirds of patients do not completely recover after strokes, while one-third cannot walk without assistance. Furthermore, in hemi-paretic subjects, who can still walk, gait efficiency is reduced and the energy cost of the gait is increased compared with efficient symmetric gait. In addition to the loss of central trophic effects and transynaptic degeneration of lower motor neurons, post-stroke skeletal muscle changes can also potentially contribute to disability. These changes include fibre-type shift in the paretic (=contro-lateral) side, increased intra-muscular fat (myosteatosis) substituting muscle tissue, spasticity, disuse, malnutrition and muscle unloading. Previous study showed that skeletal muscles of sub-acute stroke patients are subject to a persistent systemic inflammatory state, which could lead to hypercatabolism (i.e. protein degradation is higher than protein synthesis). This inflammatory state of the unaffected side could contribute to patient disability by inducing a loss of both muscle mass and strength, which leads to patient disability. This problem is particularly relevant in dysphagic patients. Therefore, the need exists to identify new compositions able to reduce the above mentioned problem.